Related Experiment Video
Updated: Jun 20, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
IGF-1 and retinopathy of prematurity in the preterm infant
1Department of Ophthalmology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. lois.smith@childrens.harvard.edu
Insights
Restoring insulin-like growth factor 1 (IGF-1) to in utero levels may prevent retinopathy of prematurity (ROP). Low IGF-1 after birth leads to retinal vascular loss and ROP development.
Area of Science:
- Ophthalmology
- Neonatology
- Developmental Biology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of childhood blindness.
- Current treatments for ROP, like retinal ablation, have poor visual outcomes.
- Understanding ROP's pathophysiology is crucial for developing preventive therapies.
Purpose of the Study:
- To investigate the roles of insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) in ROP.
- To examine the involvement of IGF-1 and VEGF in retinal vessel loss and proliferation phases of ROP.
Main Methods:
- Utilized a mouse model of ROP.
- Conducted clinical studies.
- Analyzed the relationship between IGF-1, VEGF, and retinal vascular changes.
Main Results:
- IGF-1 is essential for maximal VEGF-driven vascular endothelial cell proliferation and survival.
- IGF-1 levels are reduced in premature infants, predisposing them to retinal vascular loss.
- Deficient IGF-1 contributes to the development of ROP.
Conclusions:
- Restoring IGF-1 levels to those found in utero may serve as a preventive strategy for ROP.
- IGF-1 replacement therapy could mitigate ROP-related blindness.
Background:
Retinopathy of prematurity (ROP) continues to be a major cause of blindness in children. Although ablation of the retina reduces the incidence of blindness by suppressing the neovascular phase of ROP, the visual outcomes after treatment are often poor. Preventive therapy is required and will likely come from a better understanding of the pathophysiology of the disease.
Objectives:
To study the role of insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) in both the proliferative phase of ROP (phase II) and in the early phase when blood vessels are lost.
Methods:
Using both a mouse model of ROP and clinical studies the relationship between IGF-1, VEGF and both vessel loss and vessels proliferation in the retina was studied.
Results:
IGF-1 is required for maximum VEGF activation of vascular endothelial cell proliferation and survival pathways. IGF-1 levels are deficient after premature birth, setting the stage for retinal vascular loss and ROP.
Conclusions:
Restoration of IGF-1 to levels found in utero may help prevent ROP.
